ArticleThe Journal of cell biology1995
pp60c-src is a positive regulator of growth factor-induced cell scattering in a rat bladder carcinoma cell line.
Article in The Journal of cell biology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
27 citing papers in PubMed, 79 citations in OpenAlex.
- The inositol phosphatase SHIP2 enables sustained ERK activation downstream of FGF receptors by recruiting Src kinases.Science signaling · 2018Article
- ZDHHC3 Tyrosine Phosphorylation Regulates Neural Cell Adhesion Molecule Palmitoylation.Molecular and cellular biology · 2016Article
- cAMP Promotes Cell Migration Through Cell Junctional Complex Dynamics and Actin Cytoskeleton Remodeling: Implications in Skin Wound Healing.Stem cells and development · 2015Article
- A Network Map of FGF-1/FGFR Signaling System.Journal of signal transduction · 2014Review
- Cigarette smoke extract stimulates epithelial-mesenchymal transition through Src activation.Free radical biology & medicine · 2012Article
- The role of MAPK in drug-induced kidney injury.Journal of signal transduction · 2012Article
- Oncogenic signaling by tyrosine kinases of the SRC family in advanced colorectal cancer.American journal of cancer research · 2012Article
- A cell-based small molecule screening method for identifying inhibitors of epithelial-mesenchymal transition in carcinoma.PloS one · 2012Article
- Distinct interactions between c-Src and c-Met in mediating resistance to c-Src inhibition in head and neck cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2011Article
- Focal adhesion kinase regulates cell-cell contact formation in epithelial cells via modulation of Rho.Experimental cell research · 2008Article
- Potential molecular mechanism for c-Src kinase-mediated regulation of intestinal cell migration.The Journal of biological chemistry · 2008Article
- Src regulates cell cycle protein expression and renal epithelial cell proliferation via PI3K/Akt signaling-dependent and -independent mechanisms.American journal of physiology. Renal physiology · 2008Article
- The role of integrins in cancer and the development of anti-integrin therapeutic agents for cancer therapy.Perspectives in medicinal chemistry · 2008Article
- Elevated c-Src is linked to altered cell-matrix adhesion rather than proliferation in KM12C human colorectal cancer cells.British journal of cancer · 2002Article
- Mechanisms in epithelial plasticity and metastasis: insights from 3D cultures and expression profiling.Journal of mammary gland biology and neoplasia · 2002Review
- Article
- Phosphorylation of tyrosine residues 31 and 118 on paxillin regulates cell migration through an association with CRK in NBT-II cells.The Journal of cell biology · 2000Article
- Src is required for cell migration and shape changes induced by fibroblast growth factor 1.Oncogene · 1999Article
- Morphological differentiation of oligodendrocytes requires activation of Fyn tyrosine kinase.The Journal of cell biology · 1999Article
- Src family kinases are required for integrin but not PDGFR signal transduction.The EMBO journal · 1999Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The NBT-II rat carcinoma cell line exhibits two mutually exclusive responses to FGF-1 and EGF, entering mitosis at cell confluency while undergoing an epithelium-to-mesenchyme transition (EMT) when cultured at subconfluency. EMT is characterized by acquisition of cell motility, modifications of cell morphology, and cell dissociation correlating with the loss of desmosomes from cellular cortex. The pleiotropic effects of EGF and FGF-1 on NBT-II cells suggest that multiple signaling pathways may be activated. We demonstrate here that growth factor activation is linked to at least two intracellular signaling pathways. One pathway leading to EMT involves an early and sustained stimulation of pp60c-src kinase activity, which is not observed during the growth factor-induced entry into the cell cycle. Overexpression of normal c-src causes a subpopulation of cells to undergo spontaneous EMT and sensitizes the rest of the population to the scattering activity of EGF and FGF-1 without affecting their mitogenic responsiveness. Addition of cholera toxin, a cAMP-elevating agent, severely perturbs growth factor induction of EMT without altering pp60c-src activation, therefore demonstrating that cAMP blockade takes place downstream or independently of pp60c-src. On the other hand, overexpression of a mutated, constitutively activated form of pp60c-src does not block cell dispersion while strongly inhibiting growth factor-induced entry into cell division. Moreover, stable transfection of a dominant negative mutant of c-src inhibits the scattering response without affecting mitogenesis induced by the growth factors. Altogether, these results suggest a role for pp60c-src in epithelial cell scattering and indicate that pp60c-src might contribute unequally to the two separate biological activities engendered by a single signal.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.